Mol Microbiol 2004, 54:994–1010.CrossRefPubMed

37. learn more Knodler LA, Vallance BA, Hensel M, Jackel D, Finlay BB, Steele-Mortimer O: Salmonella type III effectors PipB and PipB2 are targeted to detergent-resistant microdomains on internal host cell membranes. Mol Microbiol 2003, 49:685–704.CrossRefPubMed Authors’ contributions KLE performed cell culture, RNA extraction, and RT-PCR. CYZ performed RT-PCR and data analysis. MZ, HB, and SZ drafted the manuscript. All authors read and approved the final manuscript.”
“Background Mosquitoes transmit many infectious diseases, including malaria, lymphatic filariasis, yellow fever, and dengue. Among these diseases, malaria is by far the most costly in terms of human health. It is endemic to more than Selleck NVP-HSP990 100 countries and causes 550 million cases per year, with the highest mortality in children from sub-Saharan Africa. Malaria transmission to humans requires a competent mosquito species, as Plasmodium parasites must undergo a complex developmental cycle and survive the defense responses of their insect host. In Africa, Anopheles gambiae is the major vector of Plasmodium falciparum infection,

AZD9291 order which causes the most aggressive form of human malaria. The Plasmodium berghei (murine malaria) model is one of the most widely used experimental systems to study malaria transmission. Gene silencing by systemic injection of double-stranded RNA (dsRNA) has proven to be a very useful tool to carry out functional genomic screens aimed at identifying mosquito genes that mediate anti-parasitic responses. In general, Anopheles gambiae is considered to be susceptible to P. berghei infection, because a high prevalence of infection can be achieved and parasites are only rarely melanized; however, silencing of either thioester-containing protein 1 (TEP1) [1], leucine-rich repeat immune protein 1 (LRIM1) [2], or LRIM2 (also called APL1, [3]), enhances P. berghei infection by 4–5 fold; indicating that, when these effector molecules are present, about 80% of parasites are eliminated by a lytic mechanism[1]. It is well documented that An. gambiae mosquitoes have a different transcriptional response to infection with P. berghei and P. falciparum

[4, 5] and genes such as LRIM1 and C-type lectin 4 (CTL4) [2], which Ureohydrolase limit or enhance P. berghei infection, respectively, do not affect P. falciparum infection in An. gambiae [6]. This raises the possibility that some antiplasmodial genes identified using the P. berghei malaria model may not be relevant to human malaria transmission. More than 400 species of anopheline mosquitoes have been identified, but only 40 of them are considered to be important disease vectors [7]. Different anopheline species and even particular strains of mosquitoes vary widely in their susceptibility to infection with a given Plasmodium parasite species. For example, twelve different strains of Anopheles stephensi have been shown to have very different susceptibility to P.